This is an archive version of 'Psychedelic Information Theory' Alpha chapters. The final version of this text can be found at:

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Chapter 12: Psychedelic Information Theory

It may seem rudimentary at this stage of our discussion to point out that different hallucinogenic drugs do indeed produce different neurochemical interactions within our brains, but this is a fact that is either missed or too often overlooked when talking about psychedelics in general. Some people consider psychedelics to be only the classic tryptamines and phenethylamines, other people would broaden the category to include dissociatives like ketamine and dextromethorphan (DXM); delirients like atropine and scopalamine found in Daturas and belladonnas; muscimol, the active compound of the fly agaric toadstool; the structurally unique active compounds of the Salvia divinorum mint; the "hypnotics" and MAO-inhibiting betacarbolines of the yage vine and peganum harmala seeds; alcohol, tobacco and THC; kava, khat, gotu, beetle nut, and hundreds of other random plants, fungi, frog extracts, industrial solvents, trade narcotics, designer pharmaceuticals, etc., etc. Each one of these drugs may be "psychedelic" in the sense that they move the mind to some elevated state which lends itself to novel thought, action, or emotive states, but each one of these drugs — even the narrow band of classic psychedelics — elicit widely different effects on the brain. And since this text is an extended digression on the fluctuations of signal flow through the mammalian neocortex, it will be useful to understand just how these different drugs are classified and what their direct methods of action are.

5-HT2A agonists: The Classic Psychedelics

We have already gone into a fair amount of detail on the classic psychedelics so we won't go over all that ground again. However, it should be noted that the phenethylamines and tryptamine psychedelics are classified more or less by their structural similarity to our endogenous amines like seratonin and dopamine. The suspected method of interaction is dynamic interruption in both serotonergic and dopaminergic systems via direct action at various receptor sites, most noticeably the 5-HT2A receptor sub-type in the cerebral cortex. At low to moderate doses they elicit an amphetamine like rush of energy coupled with a state of heightened sensory awareness. At high doses they produce profound hallucinations and can be somatically overwhelming. Although this category of drugs is the primary focus of this text, it is by no means the only drugs used to produce classically "psychedelic" effects, such as hallucinations, boundary dissolution, mystical experience, etc.

Empathogens and Entactogens: The Lesser Psychedelics

I mention this category in passing because it is helpful to know the effects of the class of drugs sometimes known as entactogens or empathogens, which means they act as sensory (entacto) and emotional (empatho) stimulators. I know some may get on my case for placing these in a "lesser" category, but I do so because this category of drug stimulates only some of the classic psychedelic effects (such as boundary dissolution, amplified emotional response, and enhanced sensation), but is missing others (such as profound or immersive hallucinations). Empathogens are typically substituted amphetamine derivatives (such as MDMA) which act as broad 5-HT (serotonin) releasers, or act in some way to flood the brain with seratonin. Entactogens are also typically substituted amphetamine derivatives that act as dopamine and/or norepinephrine releasers. I suspect empathogenic and/or entactogenic response can be generated by any drug which stimulates aminergic response in the brain, and any drug which temporarily increases the brain's supply of seratonin (such MDMA), or of dopamine and norepinephrine (such as amphetamines), will have a corresponding empathogenic or entactogenic effect, which is to say there will be an enhancement of emotional and sensory experience.

But these are only two aspects of the classic psychedelic state, and I would say that a great majority of non-visual tryptamines and phenethylamines fall into one or both of these lesser category, and even classic psychedelic phenethylamines (like Mescaline) typically only have entactogenic or empathogenic affects unless taken at very high doses. Many full-on psychedelics (like LSD) and dissociatives (like DXM) can be entactogenic and/or empathogenic at sub-psychedelic/dissociative levels, and many lesser psychedelics can become fully psychedelic with higher dose ranges. But it should be stated clearly that if you want a fully psychedelic effect you should stick with the classic psychedelics; don't go overdosing on an empathogen or an entactogen trying to make it do something it is not very good at. The side effects of this kind of high dose-range experimentation with empathogens or entactogens typically doesn't warrant the unwanted side effects, like sudden spikes in blood pressure, loss of consciousness, respiratory failure, and death. So once again knowing your substance, dose range, and desired outcome could make the difference between a pleasant entactogenic event, a fully psychedelic event, or a sudden death event.

NMDA Antagonists & The Classic Dissociatives

If it has taken this long for someone like me to write a text as detailed as this on the interactions of classic psychedelics, I can only imagine how long it will be until the world sees a text called "Dissociative Information Theory" which attempts to get a handle on the insatiable all-sucking bottomless pit that is the dissociative void. In Ketamine: Dreams and Realities, Karl Jansen does an admirable job of breaking down the effects of the dissociative anesthetic Ketamine, and makes a good argument for the case that Ketamine's antagonistic interaction at the NMDA receptor site artificially mimics naturally occurring near-death-experiences (NDEs) in which the user feels as if their spirit has been separated from the body and is floating though dark tunnels, soaring over angelic vistas, etc. This is a somewhat romanticized notion of the dissociative state, but close enough.

Pharmacologically dissociatives work on the general principle of interrupting or inhibiting the associative pathways of the brain, thus creating a state where various parts of the brain are isolated from each other, incommunicado, or simply not responding. The primary method of action for dissociatives is via NMDA (N-methyl D-aspartate) receptor antagonism. Like all receptor types, there are many subtypes of NMDA receptors, but NMDA is a primary binding site for glutamate, the neural "Go" signal. As you might guess, chemicals which block (or antagonize) the NMDA receptor will consequently act as inhibitors of neural signal firing, and if you successfully inhibit neural firing along the pathways which carry signal from one area of the brain to another, a dissociative effect is achieved.

Since there are many kinds of NMDA receptor subtypes there are many different kinds of dissociatives. The anesthetic dissociatives work by blocking neural signals from pain receptors before they can reach the somatosensory cortex in the parietal lobe. Although this is my own speculation, I have no doubt that hallucinogenic dissociatives work by placing the visual and spatial cortices of the brain in a state of chemically-induced sensory isolation, and once freed from the rendering confines of a hard 3D reality a boundless state-space emerges. If this sounds something like dreaming you are right, it is a lot like dreaming with more control over the level of dissociation and depth of sensory isolation you wish to achieve (mediated by dose range, of course).

The most popular of the classic dissociatives are Ketamine (a veterinary anesthetic) and dextromethorphan (DXM, the active ingredient of the cough-suppressant Robitussin) which are both structurally similar, DXM being a bit more complex. Both Ketamine and DXM are selective NMDA antagonists sold commercially, and both of these drugs can create powerful dissociative effects at high dose ranges. Surprisingly enough there are competing schools of thought in the underground community as to which of these drugs is the better dissociative for achieving psychedelic or shamanic effects, and another school of thought which doubts if there is any shamanic worth at all in these gross industrial pharmaceuticals. But, as usual, I would say it all comes down to ingestion context: what need do you have to fill? Does this drug fill it?

At low dose ranges the dissociatives actually act as stimulants. The low-dose effect is complex to explain, but as signal from the body is disrupted there is a corresponding excitation in the cortex coupled with a feeling of weightlessness and pressure being lifted from the body. Often there is a ringing, buzzing, tingling, or an anesthetic numbness that makes the body feel stronger and impervious to stress and pain. At moderate doses the dissociative becomes a classic CNS depressant or intoxicant (like alcohol), complete with loss of balance and orientation, blurring of vision, slurred or incomprehensible speech, etc. At high doses the dissociative plunges into the familiar orbit of the psychotic/dreaming/hallucinating mind in Hobson's AIM model. The states of isolated consciousness that erupt under a high-dose of dissociatives can be described as out-of-body (OBE), near-death (NDE), or very much like lucid dreaming, with recursive dream realities, false awakenings, hypnogogia, hypnophasia, loss of memory, etc., all part of the package. Under the fully depressant effect of the NMDA antagonist the body is essentially asleep, but locked in the darkened skull the mind still churns away, feedbacking through fading signal noise, spinning infinitely recursive visions of potential realities as it spirals into boundless oblivion...

As a personal side note, I think there is a lot to be learned about the brain and the mind through the dissociative state. More than any other drug (psychedelics included), dissociatives truly shine a light on the fact that things like "self," "identity," and "personality" are really nothing more than a group of localized sensory-processing subroutines all running in networked parallel. When you "knock out" one or more of the aspects of self via the dissociative state the other pieces become self-aware task-specific sub-units of what was once a holistic/holographic "personal mind." Thus the personal state splinters, allowing intra-personal sub-units and in some cases transpersonal meta-units of consciousness to erupt. This first-person deconstruction and reconstruction of self under the influence of Ketamine was referred to as metaprogramming by the professional consciousness explorer John Lilly, and it is very easy to see why a drug like Ketamine would seem useful in this capacity. However, there is metaprogramming and there is drug addiction and abuse, and with Ketamine one lends itself to the other quite nicely. For some reason the deconstructed self is infinitely cooler and more fun to explore than the fully constructed self, and with Ketamine you can repeat this deconstructive-reconstructive metaprogramming exercise over and over again all day every day until you run out of drugs and/or money, so there are some obvious dangers here.

But as shamanic tools go these agents are very powerful. Metaprogramming, deconstruction of self, transpersonal insights, these are all classic psychedelic boundary dissolutions happening at full effect in the dissociative state, coupled with a range of moderate to totally immersive lucid-dreamlike hallucinations which can bring the fully psychedelic response to the fore. Again, though dissociatives work in a very different way than classic 5HT2A agonists, they can still achieve a classically psychedelic effect at the proper dose range.

Datura, Belladonna, Tropane Delirients, Dramamine, Benadryl, Antihistamines & The Classic Anticholinergics

Well, okay, you wanted weird territory, here it is. Of all the families of classic hallucinogens the anticholinergics are gateways to the world of the Bizarro shaman, the one who likes to bend reality as far as it can go, the one who might not come back the same way ever again. Of all the hallucinogenic substances known to humans these are possibly the oldest, most powerful, as most dangerous to use. Found naturally in the Solanaceae family of white trumpeting-flower plants (such as Datura, Belladonna, Deadly Nightshade, Brugmansia, Jimson Weed, etc.) the tropane delirients atropine and scopalamine have been used by witches, shamen, and physicians alike for as far as recorded history goes back. Unlike the classic psychedelics which typically lead to perceptual distortions and lucid dream-like states, high dose anticholinergic ingestion leads to frank or concrete hallucination, which is the waking sensation that something or someone is right in front of you when in reality there is nothing there at all, or of believing that you are in one place when in fact you are somewhere completely different. Yet with anticholinergic hallucinations there is no doubt that what the user is seeing is not real, the acceptance of the dream-like delusion is total. The user simply forgets all previous waking contexts and accepts the paradoxical un-reality as reality, and for the most part retains little or no memory of it once it has passed. This is generally called delirium, delusion, or dementia, but experientially it is just plain strange. In a very real sense the user in the anticholinergic trance is sleepwalking: both fully awake and functioning in the real world while at the same time dreaming as if the brain were in deep REM sleep. How is that possible?

Well, first it is useful to know that anticholinergics disrupt the activity of acetylcholine at the muscarinic receptors of the cholinergic system, hence the name anti-cholinergic (and yes, it is called the muscarinic receptor because muscimol, the active compound of fly agaric mushrooms, has a high affinity for this receptor type, but as an agonist). Knowing that anticholinergics disrupt acetylcholine activity, if we look at Hobson's AIM model to try to figure out how anticholinergics work there might be some confusion. If acetylcholine is supposed to mediate sleep and REM activity, how can a drug that blocks the action of acetylcholine produce such profound dream-like effects? Once again this is a question not of action, but of dosage.

But before we get into a full clinical examination, it should be noted that experimenting with even extremely small amounts of tropane alkaloids is unpleasant. Of all the drugs mentioned in this text nothing disrupts the body's internal systems more than the tropane delirients. Motor control and mucus production go down, respiration and heart rate goes up. Common side effects include dry irritated throats, itchy skin, headaches, pressure in the head, blurred vision, pupil dilation, agitation, high blood pressure, and more. If you ever take a large dose of an anticholinergic it becomes exceedingly obvious that acetylcholine is a very important neurotransmitter, important for far more than just mediating sleep and dreaming. It is the workhorse messenger of the parasympathetic nervous system, interacting with both involuntary heart muscles and voluntary skeletal muscles to relax muscle tone and slow heart rate; it is intricately connected to stimulation of the glossopharyngeal, facial, and vagus nerves; it triggers production of saliva and mucous essential for eating, swallowing, and digestion; it is essential to long term memory formation and recall; and if your body runs low on acetylcholine it can lead to Alzheimer's disease. And although anticholinergics have been in wide use for at least thousands of years, they are by no means "safe" to use at what would be considered psychedelic doses. They are extremely dangerous to say the least.

So now that we've gotten that out of the way, let's take a look at what happens under a heavy dose of these bad boys. Under heavy Datura intoxication you essentially become a sleepwalker. A bloodshot-eyed, dry mouth, stumbling, agitated, delusional zombie. When looking at Hobson's AIM model it is hard to tell where this state actually is. It sounds like there is high acetylcholine action because of the dreamlike intensity, but obviously the user should be in a low cholinergic state if their acetylcholine uptake was massively disrupted, right? Both experientially and behaviorally it seems obvious that functions of the prefrontal cortex (contextualization of self) and hippocampus (memory formation and recall) are totally disrupted, indicating low aminergic modulation. But let's not forget that these areas also have high concentrations of muscarinic receptors which are responsive to acetylcholine, and an interruption at those sights might be enough to knock these areas into extremely low functioning states. And while dream-like frank hallucinations would seem to indicate high cholinergic functioning, this is not necessarily the case. To me it seems that there can be one of a couple things going on here...

First of all, Hobson's AIM model could be a little off the mark on a critical axis, and high acetylcholine modulation is not actually a requirement for dream activation. It could be that acetylcholine acts as both a dream promoter when aminergic functioning in the prefrontal cortex and hippocampus is low (while sleeping, resting), while conversely acting as a dream inhibitor when aminergic functioning is high (while waking, active). If we were to view acetylcholine as having a dualistic gating function on memory (waking memory input) and dreaming (sleeping memory compression) located at the hippocampus and mediated by environmental factors — such as the activity of the pre-frontal cortex, the levels of seratonin and melatonin, rhythmic circadian stimulation from the hypothalamus, etc. — then the picture becomes a little clearer. With this model any significant disruption of acetylcholine would disrupt the waking/memory sleeping/dreaming dichotomy, and thus the thin chemical boundaries which normally prevent the dreaming mind from intruding on the waking mind vanish. This model is not as clean as the pure aminergic/cholinergic duality in Hobson's unified theory, but as many chemical messengers have multiple functions in different contexts, this model or some variation on it is not entirely out of the question.

The other possibility, of course, is what I would call the boomerang effect of extreme acetylcholine interruption. Since acetylcholine is such an important messenger it is reasonable to expect that any major disruption in acetylcholine uptake would of course lead to an increase of endogenous acetylcholine production. If uptake is critically blocked the body may in turn totally freak out and begin pumping acetylcholine like mad, flooding the brain and body with as much as it can produce. And then, once the anticholinergic agent begins to metabolize... Wham! Acetylcholine smashes into the system like a runaway truck and transports the user seamlessly and instantaneously into a fully interactive waking dream-space. The acetylcholine boomerang effect was perfected by the amateur consciousness explorer Zoe 7, and detailed in his graphic autobiographical work entitled Into the Void. Within the pages of Into the Void Zoe 7 found many different ways to induce this boomerang effect on himself, including depriving himself of REM sleep for days on end and then ingesting a massive amount of Benadryl, which contains the antihistamine diphenhydramine, which also acts as an anticholinergic at high doses. Zoe 7 also used various different drugs and light-and-sound emitting brain machines (pulse generators) to amplify his technique, and this extreme REM deprivation coupled with the extreme anticholinergic action created what he subjectively believes to be complete dimensional shifts to parallel universes. The immersive states Zoe 7 produced were so profound he has now written two books about his visitations to alternate dimensions, and speaks around the world about his experiences. I'll talk more about parallel dimensions and alternate universes later, but what we are seeing here in this boomerang effect is more likely a profound immersive state brought on by a flood of acetylcholine hitting a REM deprived brain and forcing it into dream psychosis.

One might wonder why, during an intense acetylcholine boomerang action, isn't the memory also enhanced? Why does dreaming come to the fore and memory diminish? In this case in may be helpful to think of the hippocampus as a VCR for memory recording and dream playback (which may be accurately described as a kind of memory compression). Generally if the hippocampus is involved in dream activity it cannot simultaneously be recording memories of the event. This is primarily because the pre-frontal cortex is offline in the dreaming state, and cannot prime memories for delivery to the hippocampus for storage. The exception to this rule is, of course, the lucid dream state where the personal awareness of the PFC comes back online within the dream, as in the last few moments of dreaming upon waking up, where memories of dreams become more intense. In these fleeting transitional states the hippocampus can be both producing dream activity and taking memory info from the PFC at the same time. Thus the circuit from memory to dream and back to memory is completed, and acetylcholine is needed for every step of this functioning. Typically in an anticholinergic dream state there is no memory of what is happening to you. Zoe 7 claims that his use of brain-stimulating machines helped balance the acetylcholine boomerang effect and allowed him to retain enough lucidity to have a clear memory of each breakthrough episode, but I cannot personally verify that his methods actually work. Again, your mileage may vary.

Some limited personal experimentation with Zoe 7's techniques (modified for us normal humans, of course) have definitely led me to some of the most profound lucid dreaming experiences I have ever had, but that is clearly what they were. I have been in enough lucid dreams to realize when I am in one, but these were some of the crispest and most impressively detailed dreams I have ever been in, and by far the longest lasting (which is what made it both cool and exasperating at the same time). I kept walking around and knocking on things, feeling things, testing to see if everything was solid, knowing I was in a dream and that none of it was real. I was exhausted and wanted to wake up so I could get some sleep (get that?) and was not be able to, and was not able to fully get my bearings at all. Recursive realities fooled me into thinking I had retuned a couple times, when in fact I was still out of it. It was a very uncomfortable ride, totally immersive, totally wrapped like an onion, impossible to get out, insane at points. But I eventually passed out and fully crashed into zonk-land, and then it was over. It was an alternate universe all right, but one that I was happy to finally wake up from.

However, Zoe 7 must be made of stouter stuff that I am. It is his testimony that being rigorous about the REM deprivation and staying awake through the extreme somatic heaviness of all the antihistamines is the only way to break through into the fully waking dimensional shifting state. I personally cannot stand to go without REM sleep for too long, and when I start having totally immersive lucid dreams that's when I know I have been fatigued and depriving my body of sleep for too long. My own mild anticholinergic experiments can be considered a mere fraction of what Zoe 7 put himself through in the name of science, and you can say that he came back somewhat fractured (for the better?).

So that's the tale of the Bizarro shaman, Crazy Kieri and his gang of alternate world-walkers, god talkers, witches on broomsticks, and those who seek the mystic vision in the hardest and most immersive forms. A little sleep deprivation here, a pinch of anticholinergic there, wham-o presto you are in your own little universe. Again, this is not a classical psychedelic experience like you would get from a 5HT2A agonist, but it is without a doubt the farthest anyone has mapped out there on the rim of human experience, beyond psychedelic you might say. The craziest shamen are the ones who drop datura in their ayahuasca brew, for the visions, no? Oh yes, the visions. If you want to give your gods physical form, then yes, here it is, that is the recipe. But beware, you will be giving your gods physical form, and will be doing so at the risk of your own health and sanity. Triple light-speed oblivion express to the universal dream space academy, first class, yes sir. You'll receive your official badge and uniform once you get there. You can trust me on that...

So Many Drugs...

While this section has focused primarily on three major classes of hallucinogenic drugs — 5HT2A agonist psychedelics, NMDA antagonist dissociatives, and anticholinergic delirients — as well as providing a little info on the non-hallucinogenic entactogens, there are still many other substances that produce psychedelic effects that I have left out. For example, The Salvinorin terpenes derived from the Central American mint Salvia divinorum, are without a doubt extremely psychedelic when vaporized and inhaled. They produce boundary dissolution, perceptual distortions, hallucinations, etc., but of a type unlike any of the others mentioned so far. Interestingly enough, these substances appear to be a kappa-opioid receptor agonist, which means they increase activity at the kappa-opioid receptor, which is distributed widely throughout the central nervous system with high density in brainstem and limbic regions. I would suspect that by acting as a kappa-opioid agonist in the temporal lobe, limbic system, and brainstem the Salvinorin terpenes (and other kappa-opioid agonists) act as both amplifiers and distortion filters of somatic signal traveling from the lower subconscious/emotional brain to the higher rational brain, thus producing bottom-up perceptual effects originating in the lower brain.

The perceptual effects of Salvinorin terpenes — such as a hard tingling sensation, rotation of spatial orientation, dissociative boundary dissolution, the emergence of geometric or cellular patterns, somatically overwhelming immersive states — all suggest typical psychedelic activity in the cortex, but could also be caused by targeted dissociation or signal disruption within various brainstem/limbic regions. We'll look at these kinds of interactions in more detail throughout this text, but the fact that kappa-opioid receptors (KORs) can mediate psychedelic or psychotomimetic effects shows once again that psychedelic effect is not always mediated by one particular interaction at one particular receptor subtype. In fact, the more you look at it, the more you realize that disruption of any neural messenger significant enough to cause excitation of and/or dissociation between various sensory processing areas of the brain is all that is needed to cause one or many types of classically psychedelic effect. Even alcohol, for instance, can be used for lesser psychedelic effect: it dissolves boundaries, distorts perception of self and others, and amplifies emotional salience of sensation. So really, when you get right down to it, lots of things are psychedelic in some way, even if they are not classic psychedelics.

Knowing what class each type of hallucinogen falls into, how it works, and understanding how it produces its visionary effect is arguably the most important task of the shaman. In modern terms, hallucinogenic psychopharmacology is a sub-specialized field of pharmacology in general, and anyone can pick up the basic knowledge with a few years of continuing study. They even offer degrees for this kind of thing now, diplomas and everything, and you can even get a job with a degree like that, though probably not working with psychedelics directly (though there is always the outside chance). The information offered in this text is really just the most basic overview of the field, but only as it relates to psychedelic and hallucinogenic phenomena. For the student seriously seeking to study shamanism, one should seek out as much information as possibly on pharmacology, the various classes of drugs, how they work, and what their side effects are before ever experimenting with any extreme techniques or dose ranges. The knowledge is out there and easy to find. You have no excuse for ignorance. You have been warned.

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